The study of defective repair of MNNG-(N-methyl-N'-nitro-N-nitrosoguanidine) produced damage was extended. One-fifth (17/88) of the human tumor cell strains tested comprises a group of cell strains (Mer-) that differs from the remaining 71 tumor strains (Mer+) or from normal human fibroblasts (also Mer+) in the following ways: 1) inability to excise O6-methylguanine from their DNA after being treated with MNNG; 2) relative inability to support the growth of MNNG-damaged adenovirus 5; and 3) sensitivity to being inactivated by MNNG or BCNU (Bis-chloroethyl-nitrosourea) in a reproductive way. The results may be relevant to uncovering the molecular reasons for success of certain bifunctional alkylating chemotherapeutic agents (BCNU, CCNU).